Scn4b Double Nickase Plasmid (h): sc-411001-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Scn4b Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- Scn4b Double Nickase Plasmid (h) and Scn4b Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SCN4B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Scn4b Double Nickase Plasmid (h) | sc-411001-NIC | 20 µg | $410.00 | |||
Scn4b Double Nickase Plasmid (h2) | sc-411001-NIC-2 | 20 µg | $410.00 |
SCN4B encodes the sodium channel β4 subunit (Scn4b), an auxiliary membrane protein that associates with voltage-gated sodium channel α subunits to influence channel gating, cell-surface expression, and excitability. Beyond modulating action potential firing, SCN4B has been linked to regulation of cell adhesion and signaling through interactions at the plasma membrane that can impact cytoskeletal organization and membrane microdomain composition. Altered SCN4B expression or variants are studied in the context of excitability-related disorders and dysregulated electrical signaling, including cardiac and neuromuscular phenotypes. In cancer biology, SCN4B has also been investigated as a modulator of migration and invasion programs, making it relevant to pathways governing epithelial–mesenchymal transition and metastatic behavior.
Scn4b Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SCN4B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SCN4B. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt SCN4B function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of SCN4B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.